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. 2019 Jan 23;9:336. doi: 10.1038/s41598-018-36728-y

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Molecular pathways that regulate sVEGFR1-i13 expression in endothelial and SQLC cells. (a) In endothelial cells, both positive (hypoxia, U2AF65 splicing factor) and negative (JMJD6, NOTCH1) regulators of sVEGFR1-i13 expression have been described in response to VEGF-A (VEGF₁₆₅) stimulation. (b) In squamous lung carcinoma cells, anti-angiogenic therapies increase the intra-cellular level of VEGF₁₆₅. VEGF₁₆₅ induces the expression of the transcription factor SOX2 which controls SRSF2 protein level by binding to the SRSF2 promoter. As a final step, SRSF2 controls the alternative splicing of VEGFR1 towards sVEGFR1-i13 expression.